Neuro Flashcards
L3 root compression? (4)
Sensory loss over anterior thigh
Weak quadriceps
Reduced knee reflex
Positive femoral stretch test
L4 root compression? (4)
Sensory loss over anterior knee
Weak quadriceps
Reduced knee reflex
Positive femoral stretch test
L5 root compression? (4)
Sensory loss over dorsum of foot
Weakness in foot and big toe dorsiflexion
Reflexes intact
Positive sciatic nerve stretch test
S1 root compression?
Sensory loss over posterolateral aspect of leg and lateral foot
Weakness of plantarflexion
Reduced ankle reflex
Positive sciatic nerve stretch test
When to consider MRI for root compression?
If symptoms persist for 4-6 weeks despite analgesia, physiotherapy and exercises
Initial signs of SACD development in B12 deficiency (e.g. 2 years after gastrectomy for cancer)? (3)
Loss of ankle reflexes
(knee reflexes may be brisk)
Loss of vibration and pin prick
Wide-based ataxia
Difference between migraine symptoms in kids and adults? (3)
In kids shorter lasting, more commonly bilateral, and GI disturbance more prominent
Can aura for migraine occur without headache?
3 things which make the sensory/motor disturbance an aura?
Yes
- Fully reversible
- Develop over at least 5 mins
- Last 5-60 mins
5 common migraine auras?
- Double vision
- Visual symptoms affecting one eye (scintillating scotoma)
- Motor weakness
- Poor balance
- Decreased level of consciousness
Becker/Duchenne MD:
- inheritance? problem with what gene?
- Symptoms they have in common? (3)
- Differences between them? (2)
- Difference between these and myotonic dystrophy?
Autosomal Dominant
Dystrophin gene - large membrane protein which attaches membrane to actin in muscle
- Progressive proximal muscle weakness
- Calf pseudohypertrophy
- Gower’s sign: child uses arms to stand from squatted position
- Duchenne onset from 5 y/o, Becker’s is later in teens
- 30% in Duchenne have intellectual impairment, this is very rare for Becker
Myotonic dystrophy - muscles have increased tone, unable to relax
What muscles are generally spared in MND?
Extraocular - eye movements spared
Loss of thumb abduction after colles #?
Median nerve injury
How does ulnar nerve damage present in hand?
Weakness of 4th and 5th fingers, with loss of sensation of these fingers also front and back
MRI with/without contrast should be used for demyelinating lesions e.g. MS?
What is seen on MRI with MS?
On CSF?
WITH contrast
MRI:
- High signal T2 lesions
- Periventricular plaques
- Dawson fingers: hyperintense lesions perpendicular to corpus callosum extending up like little fingers
CSF:
- Oligoclonal bands
- Increased intrathecal synthesis of IgG
5 month old with seizures and developmental delay - EEG shows hypsarrhythmia?
What is the typical seizure of this condition like?
Prognosis?
Infantile spasms (West Syndrome)
Salaam attacks - flexion of head, trunk and limbs with extension of arms
(lasts 1-2 secs and repeated up to 50 times)
Poor prognosis - progressive mental handicap
What diet is good for treatment-resistant epilepsy in kids?
Ketogenic
1st step in first aid of patient with raised ICP?
Head elevation to 30 degrees
Causes of raised ICP? (5)
Symptoms? (5)
- Idiopathic intracranial hypertension
- Traumatic head injuries
- Infection (e.g. meningitis)
- Tumours
- Hydrocephalus
Headache Vomiting Reduced consciousness Papilloedema Cushing's triad - widening pulse pressure, bradycardia, irregular breathing
Investigations for raised ICP? (3)
- CT/MRI key to see underlying cause
- Increased opening pressure on LP
- Invasive - catheterisation of lateral ventricle to measure pressure
Management of raised ICP?
(Ix and treat underlying cause)
- Head elevation to 30 degrees
- IV mannitol
- Controlled hyperventilation (reduce pCO2, cerebral vasoconstriction, temporary lowering of ICP)
- Removal of CSF (e.g. repeated LP in idiopathic ICH, or ventriculoperitoneal shunt)
Is Guillain Barre painful? Cranial nerve involvement? Autonomic involvement? Why can papilloedema occur? Ix? (2)
65% experience back/leg pain
Cranial: diplopia, bilateral facial nerve palsy, oropharyngeal weakness common
Autonomic: urinary retention, diarrhoea
Papilloedema: decreased CSF resorption
Ix:
- LP: raised protein but normal WBC
- nerve conduction studies: decreased motor nerve velocity
Apart from weakness, what other symptoms can people get with Bells’ palsy?
Management? (2)
When should they show signs of improvement?
Prognosis?
- Post-auricular pain (often precedes paralysis)
- Altered taste
- Dry eyes
- Hyperacusis
- Prednisolone PO within 72 hours of onset
- artificial tears and eye lubricants
<3 weeks - if not improvement refer urgently to ENT
Most recover fully in 3-4 months, if untreated 15% have permanent mod-sev weakness
Should prokinetics e.g. metoclopramide be used in kids with GI disturbance in migraines?
No - they should be used with extreme caution in kids due to common SE of asthenia, parkinsonism and depression
(reserved for chemo etc)
(also they are generally CI in epilepsy)
Tuberous sclerosis:
- inheritance?
- 2 neurological features?
- 5 derm features?
- 1 in eye?
- 1 in kidney?
Autosomal Dominant
Neuro:
- Epilepsy
- Intellectual impairment
Skin:
- Depigmented ash-leaf macules (fluoresce under UV)
- Roughened patches of skin over lumbar spine (Shagreen patches)
- Angiofibromas in butterfly distribution over nose (adenoma sebacum)
- Subungal fibromas
- Cafe-au-lait macules
Eye:
- Retinal hamartoma
Kidney:
- PKD
What are the 4 Parkinsons Plus syndromes?
- Multiple System Atrophy
- Lewy Body Dementia
- Progressive Supranuclear Palsy
- Corticobasal degeneration
Apart from parkinsonism, what 3 other things are seen in progressive supranuclear palsy?
Response to drugs?
- Impairment of vertical gaze: down worse than up (complain of trouble reading/descending stairs)
- Postural instability and falls (stiff, broad-based gait)
- Cognitive impairment (frontal lobe dysfunction)
Poor response to L-dopa
Motor weaknesses in common perineal nerve injury? (3)
Sensory loss (2)
What muscle compartments will have wasting? (2)
Weakness of:
- foot dorsiflexion
- foot eversion
- extensor hallucis longus
Sensory loss:
- dorsum of foot (incl 1st web space)
- lower lateral part of leg
Wasting of:
- anterior and lateral leg compartment muscles
(anterior = deep; lateral = superficial)
What blood component is it important to check in workup of TIA? Why?
Glucose
Hypoglycaemia can cause focal neurological symptoms and mimic TIA
How is a TIA defined?
New definition is tissue based:
A transient episode of neurological dysfunction caused by focal brain, cord or retinal ischaemia, without acute infarction
Immediate management of a TIA?
Referral if suspected TIA in last 7 days?
If suspected TIA >7 days ago?
What is a crescendo TIA and what is the referral for this?
Referral if suspected cardiac/carotid source of stroke?
Driving after suspected TIA?
RULE OUT BLEED!!!
Give aspirin 300mg immediately
(unless bleeding disorder, already taking low-dose aspirin or it is CI)
- Be seen in <24 hours by stroke specialist
- Be seen asap in <7 days by a stroke specialist
Crescendo TIA = >1 TIA - admit for observation urgently
- also admit for observation urgently
Don’t drive until after being seen by specialist
Antithrombotic therapy post-TIA?
When is carotid endarterectomy performed?
Clopidogrel 1st line
Aspirin + dipyramidole 2nd line (if cannot tolerate clopiogrel e.g. diarrhoea)
- If stenosis >70% and stroke/TIA in carotid territory
How to tell if a 3rd nerve palsy is a surgical problem?
3rd nerve palsy due to posterior communicating artery aneurysm?
Other causes of 3rd nerve palsy? (5)
Pupil is dilated
Painful - pain around/behind the eye and/or generalised headache, 3rd nerve palsy and dilated pupil
- diabetes
- vasculitis (GCA, SLE) or others (MS, amyloid)
- uncal herniation through tentorium if raised ICP
- cavernous sinus thrombosis
- Weber’s syndrome: ipsilateral 3rd nerve palsy with contralateral hemiplegia - midbrain stroke
Post-LP headache:
- when does it come on?
- how long does it last?
- what position is it worse in?
- if it doesn’t resolve in set time period?
24-48 hours (occurs due to low pressure)
- <72 hours
- worse when upright (better lying down)
- If >72 hours then treatment indicated to prevent subdural haematoma:
blood patch, epidural saline or IV caffeine
Scoring system for suspected stroke?
After FAST
ROSIER:
First exclude hypoglycaemia, then stroke is likely if any of the following:
- LOC/syncope
- Seizure activity
- Asymmetrical facial, arm or leg weakness
- Speech disturbance
- Visual field defect
Ix for suspected stroke?
Non-contrast CT
Who can initiate treatment for Parkinson’s?
1st line?
Specialists only
1st line:
- if motor symptoms affect QOL: levodopa
- if not affecting QOL: dopamine agonist, MAO-B inhibitor or levodopa
Unwanted effects of levodopa? (5)
Why can it not be stopped immediately?
What type of Parkinsonism is it not used in?
Dyskinesia (involuntary writhing) 'On-off' effect Dry mouth Postural hypotension Psychosis
DO NOT stop levodopa immediately - risk of acute dystonia
NOT used in drug-induced parkinsonism
What dopamine agonists are mainly used in Parkinsons?
Why try to avoid ergot-derived ones such as cabergoline or bromocriptine?
Ropinorole or Apomorphine
Cabergoline/Bromocriptine can cause retroperitoneal, cardiac and pulmonary fibrosis. Before commencing baseline echo, creatinine and CXR should be taken and monitor patients closely
Example of a MAO-B inhibitor?
How does it work?
Selegiline
Inhibits breakdown of dopamine. Higher doses also prevent breakdown of serotonin and NA (antidepressant)
2 examples of COM-T inhibitors?
How is it used?
Tolcapone, entecapone
In conjunction with levodopa as it prevents breakdown of dopamine
What type of drugs are used for drug-induced parkinson’s?
Antimuscarinics - procyclidine, trihexyphenidyl etc
Help tremor and rigidity
For each of these where is the lesion and describe the aphasia:
- Wernicke’s?
- Broca’s?
- Conduction?
- Global?
Wernicke’s (Receptive):
- Lesion in superior temporal gyrus (MCA)
- Comprehension impaired, speech is fluent but makes no sense - ‘word salad’
Broca’s (Expressive):
- Inferior frontal gyrus (MCA)
- Comprehension normal, speech is non-fluent and halting
Conduction:
- Lesion in arcuate fasciculus (between broca and wernicke)
- speech fluent but repetition is poor - aware of errors they are making
Global:
- Lesion affecting all 3
- Severe receptive and expressive aphasia - can communicate using gestures
MS management:
- acute relapse?
- for fatigue?
- for spasticity?
- bladder dysfunction?
- oscillopsia (visual field oscillation)?
Relapse: IV methylpred 5 days - shortens relapse but no effect on recovery
Fatigue:
- Rule out anaemia, thyroid, depression
- Amantadine
- Mindfulness, CBT
Spasticity:
- Baclofen
- Gabapentin
- Diazepam, Dantrolene or Tinzadine
Bladder - urgency, frequency, overflow, incontinence etc:
1. bladder USS to assess residual volume
2. If normal residual volume, anticholinergics may help frequency
3. If significant residual volume - intermittent self-catheterisation
(be aware anticholinergics may worsen symptoms)
Oscillopsia:
- Gabapentin
DMARDs for MS?
B interferon
Glatiramer acetate - immunomodulator
Natulizumab - recombinant MAb, against leucocytes, prevents crossing of BBB
Fingolimod - prevents lymphocytes leaving lymph nodes
Hoarseness and uvula deviating to right?
Left vagus nerve lesion
uvulAWAY from side of lesion
What tracts are affected in SACD?
DCML - proprioception, vibration
Lateral corticospinal - spasticity, brisk knee reflexes, positive babinski
ankle jerks typically lost
Chronic form of Guillain barre?
Chronic inflammatory demyelinating polyneuropathy
Causes of CNIII palsy?
What is seen?
Causes:
- diabetes
- Uncle herniation through tentorium cerebelli in raised ICP
- Posterior communicating artery aneurysm (painful)
- vascular (vasculitis, cavernous sinus thrombus, Weber Syndrome - midbrain stroke)
Signs:
- down and out eyeball
- dilated
- ptosis
- pupil won’t constrict to light, but light shone in that eye causes consensual constriction
Cerebral venous sinus thrombosis: - presentation of sagittal? - cavernous? - lateral? Gold standard Ix?
All have insidious onset over hours-days of severe headache, N&V
Sagittal:
- may cause seizures and hemiplegia
- parasagittal wartershed infarcts may be seen
Cavernous:
- periorbital oedema
- ophthalmoplegia - 6th nerve before 3rd and 4th
- central retinal vein thrombosis
- 5th nerve involvement may cause hyperaesthesia of upper face/eye pain
Lateral:
- 6th and 7th nerve palsies
Ix: MRI venogram
Degenerative cervical myelopathy Ix?
Rx?
MRI
Decompression surgery - best outcome within 6 months
Physio should only be initiated by specialists as manipulation can worsen spinal cord damage
Cushing’s triad?
Bradycardia
Irregular breathing
Hypertension with a WIDE pulse pressure
Left sided facial weakness - what side and U/L motor neurone would be affected and how can you discriminate?
Left facial weakness
Right Upper motor neurone
If the forehead muscles are spared
Left Lower motor neurone
If the forehead muscles are affected
Causes of bilateral facial muscle weakness?
GBS Sarcoidosis (parotid swelling) Lyme disease Bilateral acoustic neuromas (NF2) Bell's palsy - 1% Bells Palsy are bilateral but Bells Palsy causes 25% bilateral facial weakness
Causes of LMN facial palsy?
Bell's palsy Ramsay Hunt Syndrome Acoustic neuroma Parotid tumour HIV Diabetes MS (may also cause UMN)
Can Bell’s Palsy be painful?
Yes in 50% there may be some pain
If no vesicles in ear though then not Ramsay Hunt
How to test if fluid from er/nose is CSF?
Bedside - glucose - esp in trauma
Gold standard - beta-2 transferrin (but this takes about a week to get back)
MND - features of:
- ALS?
- Primary Lateral Sclerosis?
- Progressive Muscular Atrophy?
- Progressive Bulbar/Pseudobulbar Palsy
ALS:
- UMN and LMN signs
- familial - chromosome 21
- 25% have bulbar onset
PLS:
- UMN signs only
Progressive muscular atrophy:
- LMN signs only
- Distal before proximal
- best prognosis
Progressive Bulbar Palsy:
- Palsy of muscles of chewing, swallowing and face - brainstem motor nuclei
- worst prognosis
(bulbar = LMN, pseudo bulbar = UMN of corticobulbar tracts)
Difference between spasticity and rigidity?
Spasticity:
- caused by motor tract UMN e.g. cortex, brainstem, corticospinal tract
- On quick movement there is initial resistance which melts away, no resistance on slow movement (‘clasp knife’)
Rigidity:
- caused by extrapyramidal e.g. basal ganglia
- resistance on slow movement, and doesn’t melt away on quick movement
MOA of ondansetron?
Where does it act?
5-HT3 antagonist
CTZ in the medulla
1st line management of absence seizures?
Sodium valproate or ethosuxomide
If patient is brought into A&E in a status, most important 2 causes to rule out first?
Hypoxia
Hypoglycaemia